Surgery or ? for treatment of recurrent castrate-resistant Pca
Last year, a number of you posting to this forum provided enormously valuable advice as I sorted through treatment possibilities after receiving a diagnosis of locally advanced prostate cancer (in a thread titled "Surgery or Radiation?" http://csn.cancer.org/node/258414). I'm hoping some of you can help me once again sort through the possibilities for treatment of what continues to be a complicated and very confusing case.
A brief summary: I was diagnosed at 61 yrs old in April 2013 after increasing urinary symptoms and a PSA reading of ~34 led to a biopsy; 14 of 14 cores were 50 - 100% positive for mostly Gleason 4 or 5 adenocarcinoma, evidence of perineural invasion and extension outside the prostatic capsule but negative lymph nodes and bone scan. After consulting with you guys (and gals) and a number of oncologists at several cancer centers, my wife and I opted for treatment at a NCI-designated Comprehensive Cancer Center, where I happen to work as a scientist (it's convenient to be able to walk to the clinics down the corridor from my lab . . . but this was only a minor factor in my decision to be treated where I work). I am quite fit, in part because shortly after diagnosis I began to hike up and down mountains as frequently as I could. ADT was initiated immediately followed by 81 Gy EBRT (45 fractions). There was some evidence that the tumor was castrate-resistant from the start (after initiating ADT but before beginning radiation treatment, PSA declined more slowly than usual and urinary symptoms continued to increase despite ADT to the point where I needed to catheterize to void my bladder even before radiation treatment began - and the need to catheterize continues). In January 2014, four months after radiation treatment ended, PSA had dropped to 0.34 ng/ml - not too bad all things considering. But then it headed up again; four subsequent increases between January and late June of this year brought me back up to a PSA of 2.6 with a doubling time of less than a month. The very short time to PSA nadir post radiation and the rapid doubling time pointed to an extremely aggressive castrate-resistant (and maybe radioresistant) tumor and/or systemic metastatic disease. Imaging studies (CT and MRI) suggested the primary tumor was maybe not the source of the rising PSA. Last month (July 2014), both an F18 PET bone scan and a Tech 99 bone scan detected a solitary prominent focus of radiotracer uptake on a rib. At this point everybody (well, almost everybody) thought it was likely I had graduated to Stage 4 disease. Surprisingly, however, an exhaustive analysis of this lesion by pathologists after it was resected failed to detect metastatic prostate adenocarcinoma. Instead, this lesion turned out to be a benign cartilagenous tumor. This was sort of interesting, because after discovering a lump in my leg during radiation treatment last summer, surgeons at Memorial Sloan Kettering dug a rare tumor out of my quadriceps that looked like it might be a sarcoma but also turned out to be benign. So maybe there's a connection between these two benign tumors, but we're not sure how or if they might be related to the prostate tumor.
Here's where we are now: 16 months after diagnosis, we're dealing with an aggressive, castrate-resistant (and perhaps radiation-resistant) recurrent primary tumor with parameters that usually are associated with systemic disease, but incredibly - and I'm not using this word casually - we can't find any evidence of metastasis. At the end of a recent clinical conference discussion of my case (which I attended), six clinicians voted to recommend a salvage radical prostatectomy, but this is frought with difficulites for the surgeon (in distinguishing normal from tumor tissue) and the patient (high likelihood of permanent bowel and urinary incontinence because the surgeon will have difficulty distinguishing normal from tumor tissue). I value my life more than I value bowel or urinary continence so I've been considering this option, but at the moment this seems too high a price to pay if I'm going to become metastatic anyway, which is likely to happen soon. Three clinicians at the conference voted against surgery, but there aren't many other obvious options - as one clinician said, given it's early evolution to castrate-resistance and potential radiation-resistance, it's unlikely the tumor will respond very well to any new drugs we throw at it.
So: I'm hoping that someone out there reading these posts has had or knows someone who's had a similar experience that might help to inform my thinking about how to proceed with treatment. I should add that my goal is not disease-free survival - there's little doubt that short of a miracle this is not an obtainable goal - but rather, maximum lifespan extension with as few quality of life issues as is possible. Once again, I'm very grateful for any help you might be able to provide. I wish the best of luck to all of you who are also battling this difficult disease.
Mounty
Comments
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Are you experiencing refractory? Not yet is my view
Bill
I am glad for your return to this forum. You got a difficult case but your willingness in accepting your fate, no matter the way you may use to kill the bandit, is great news. Your post shows your spirit high and positive. This is a good start for a salvage treatment.
You know that we are no “experts” in PCa affairs but a team of curious so that our opinions are from laymen answering on experiences obtained along our years of survivorship and some researches we come across.
From your descriptions I cannot see a reason to classify your case as hormone refractory or radiation resistant (which term I think it incorrect). You did not share details on the levels and times of the PSA tests to give you a better opinion, but the serum does not decrease that fast. The drugs used in the hormonal protocol also may have not driven you to castrate levels (T lower than 20 ng/dL). Many facts could be behind the reason of your results. Circulating T takes time to “clean up”.
The increase of PSA after radiation is also common in guys with the prostate in place. Localized inflammation is thought to be behind the reason of a surge in PSA. There is a phenomenon called bounce PSA that patients experience after radiotherapy with similar characteristics to those you describe. The PSA results become erratic going up and down for a period that can last 2 to 3 years after the therapy, reaching a nadir much later. Your need for catheterize to void is prove that inflammation is present. Neither ADT nor RT would improve the symptom that fast. Hyperplasia needs to be handled with due drugs.
The negative scans are good news. That is evidence that the cancer may be totally localized which aspect could be render surgery to debulk the whole gland a success. In any case, after RT the surgery may lead to nasty side effects of incontinence as you already found out. By the way, a surgeon cannot distinguish normal from tumor tissue just with the open eye. When dissecting the “flesh” they try taking the most of it to be sure that they catch the whole cancerous tissue.
My suggestion is that you give more time to ascertain of recurrence and that you continue with the adjuvant ADT protocol. You need to get a second opinion about the problem in voiding. A cystoscopy should be done to look for any restriction from the side of the bladder. The second-line hormonal drugs are more “refined” and address intratumoral aspects, and you would not lose anything in taken them if such timing comes in need in the future.
You should have the testosterone tested. Low T and high PSA is the rule to classify you as HT refractorty.
Your previous story is here;
http://csn.cancer.org/node/258414Best regards and luck in your journey.
VGama
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VascodaGama said:
Are you experiencing refractory? Not yet is my view
Bill
I am glad for your return to this forum. You got a difficult case but your willingness in accepting your fate, no matter the way you may use to kill the bandit, is great news. Your post shows your spirit high and positive. This is a good start for a salvage treatment.
You know that we are no “experts” in PCa affairs but a team of curious so that our opinions are from laymen answering on experiences obtained along our years of survivorship and some researches we come across.
From your descriptions I cannot see a reason to classify your case as hormone refractory or radiation resistant (which term I think it incorrect). You did not share details on the levels and times of the PSA tests to give you a better opinion, but the serum does not decrease that fast. The drugs used in the hormonal protocol also may have not driven you to castrate levels (T lower than 20 ng/dL). Many facts could be behind the reason of your results. Circulating T takes time to “clean up”.
The increase of PSA after radiation is also common in guys with the prostate in place. Localized inflammation is thought to be behind the reason of a surge in PSA. There is a phenomenon called bounce PSA that patients experience after radiotherapy with similar characteristics to those you describe. The PSA results become erratic going up and down for a period that can last 2 to 3 years after the therapy, reaching a nadir much later. Your need for catheterize to void is prove that inflammation is present. Neither ADT nor RT would improve the symptom that fast. Hyperplasia needs to be handled with due drugs.
The negative scans are good news. That is evidence that the cancer may be totally localized which aspect could be render surgery to debulk the whole gland a success. In any case, after RT the surgery may lead to nasty side effects of incontinence as you already found out. By the way, a surgeon cannot distinguish normal from tumor tissue just with the open eye. When dissecting the “flesh” they try taking the most of it to be sure that they catch the whole cancerous tissue.
My suggestion is that you give more time to ascertain of recurrence and that you continue with the adjuvant ADT protocol. You need to get a second opinion about the problem in voiding. A cystoscopy should be done to look for any restriction from the side of the bladder. The second-line hormonal drugs are more “refined” and address intratumoral aspects, and you would not lose anything in taken them if such timing comes in need in the future.
You should have the testosterone tested. Low T and high PSA is the rule to classify you as HT refractorty.
Your previous story is here;
http://csn.cancer.org/node/258414Best regards and luck in your journey.
VGama
VG,
Thanks for your kind words and, as always, your valuable comments. A lot has happened during the 15 months since I last posted on the earlier thread. Because the recent post you're responding to was already quite long (and because I was worried some of the details might be unnecessarily worrisome for newly diagnosed Gleason 9 or 10 patients reading this post), I skipped over some of the details. Maybe this was a mistake - I'll try to summarize the additional data as succinctly as I can:
PSA reached a nadir of 0.34 ng/ml in January; it climbed back up to 0.55 in February, 1.09 in March, 2.01 in May and 2.59 in June, and last week's reading was 6.43, although this last reading is difficult to interpret for a few reasons, including the possibility it might have been influenced by the effects of a re-biopsy of the prostate on July 1 (more about this in a moment). We (the clinicians and I) thought this might be a bounce at first, but I don't think the steady climb in multiple readings over a period of 8 months is consistent with this possibility. I also should have told you that shortly after surgery at MSK last October to extract the tumor in my quadriceps, I was clobbered by acute, systemic pain in just about every skeletal joint in my body, most likely due to muscle wasting secondary to profound weight loss (I'm now more than 40 kilos lighter than I was 16 months ago), the inhibitory effects of ADT on muscle maintenance, and prolonged inactivity after the leg surgery. Part of the solution to this problem has been a steady diet of the potent prescription-only (at least in the States) NSAID Celebrex, 200 milligram capsules twice a day. I think you're correct that inflammation is one component of the problem, because immediately after I started taking Celebrex in March, the urinary symptoms improved, but only slightly. But Celebrex doesn't seem to have had a major impact on the PSA readings.
Perhaps the most important information I left out (and this was simply an oversight) is that 9 of 12 cores taken in the July 1 biopsy were positive for high-grade (Gleason 8 and 9) malignant disease. The meaning of this is complicated by the fact that biopsies performed such a short time after radiation treatment ends (10 months in my case) are likely detecting unresolved residual disease (radiation treatment can take up to a year or more to kill tumor cells) in addition to recurrent disease. Even so, the pathologists are apparently convinced that there is plenty of recurrent tumor, which is likely contributing to the rising PSA. Testosterone has been measured in parallel with every PSA measurement - it was down to 13 in January, and the latest reading is 3 (!) - and so the ADT drugs have been effectively doing their job of chemical castration. Combined with the evidence for castrate-resistant disease that was apparent at the start of this whole adventure, this is the basis for thinking that we're dealing with an extremely aggressive, castrate-resistant tumor. Whether it's also radiation-resistant (perhaps the more frequently employed term is radio-resistant but to me this is less descriptive) is less clear - this may simply reflect my occasional discouragement that after 16 months of very aggressive therapy (ADT + maximum radiation and I've also been on the anti-androgen Casodex since last October), not much seems to have been accomplished in the battle against this tumor.
The urinary problems that require continued catheterization are something of a mystery. Celebrex improved the situation, but not by much. A cystoscopy in February detected a radiation-induced stricture, which of course we assumed was responsible for the problem. Surgery (urethrotomy) a week later followed by repeated urethral dilations effectively eliminated this stricture, which was no longer detectable in a cystoscopy performed in June, and it modestly improved symptoms (increased urine flow), but not sufficient to stop catheterizing. This most recent cystoscopy also detected a kink in my urethra that the urologists think is caused by the tumor - so this suggests that the urethra is being occluded by pressure from the tumor. I'm not convinced, however, that (as you are suggesting), inflammation isn't also part of the problem, despite the Celebrex. But I'm also not sure how to address this possibility.
I have to tell you that maintaining a positive attitude about all this is easier in the absence of evidence for metastatic disease. The absence of metastatic disease in my case is quite extraordinary, and I suspect it has something to do with the fact that I'm extremely healthy in every other respect, perhaps because of an immune system that has always very effectively fought off infectious diseases. I also think that a sense of humor about all this stuff is important, although I'm having a little more difficulty maintaining one lately. Perhaps you and others who were posting on my earlier thread remember a fellow poster to this thread, Tp23, who has a very similar case. Tp23 and I (and our wives) have become close friends, and his wicked sense of humor (which was evident in the earlier thread) has helped both of us and our families to remain reasonably sane during the 16 months since we both learned we had been attacked by the bandit.
I would be grateful for any additional thoughts you might have now that you have a more complete understanding of the situation (hopefully). You are correct to note that both of us our amateurs in this business, which means that everyone reading our posts needs to evaluate the information content carefully. Even so, I believe that your posts have been equally as helpful as the advice of experts to many, many patients - certainly this is the case for me.
Bill
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Multimodal approach
Bill
I am sorry for the comments on your status. I did not know the details and just wanted to pass you some hits that could be of help in your decisions. You are consulting a good team of physicians and they know well what the best is for you. Dr. Susan Slovin, a medical oncologist and researcher at the MSKCC, gave me precious suggestions when I recurred after surgery (2001) during a nasty “foggy” period of my journey.
I disagree with your concern for posting all the information regarding your case. The worse for cancer patients is not knowing about real facts. I correspond to other PCa forums too, but I like the CSN because it is free of “restrictions”. We can share more openly the details and aspects evolving our problem. It is good to read plain stories of the many survivors, even the nasty ones. It makes us to be more respectful to one another and become closer in the common matter.
Many of you, physicians, for whatever reason it may be, think that we patients are better if kept in the “dark”, so you tend not to be so descriptive or disclose the “baddy” of the story. However, in this forum we go against that principle and discuss openly the feelings even when complaining about our doctor’s appointments and views. Surely you are welcome with or without the concerns.You got a very difficult cancer to treat. The initial diagnosis with Gleason 9 and voluminous tumour (14 positive cores) plus positive DRE (suggesting extraprostatic invasion) made you to choose RT+ADT. I think you did well. Your fight is still going on and you need to get to a decision with the intent in holding any progression.
Your exchanged posts with Casey (http://csn.cancer.org/node/258414#comment-1368807) on the multimodal therapy approach are a good start to look at for your continuing treatment. I do not suggest surgery yet because of the loss in quality of life and because of the timing so close to RT (8 months). You can do it at a later date as the action would be debulking the gland, which in the presence of ECE does not assure complete cure but longer survival. With that in view, surgery can be done any time, though, keeping in mind that in a later date would allow the cancer to spread further (if nothing is done in-between). The recent negative image exams may consider your case localized yet.When a case becomes hormone refractory while a guy is having a traditional ADT protocol, it is so considered because the cancer starts using drugs like Casodex (antiandrogens) to satisfy its own food demand. These drugs got similar bio structures as the real stuff and they are available plenty (one is taking it) to feed on. Stopping Casodex one may experience the so called AAWR (withdrawing response). Hormone refractory in such a case should be termed antiandrogen refractory not ADA refractory.
Continuing with a LHRH agonist seems proper because it avoids the circulating testosterone. But it does not stop the cancer from availing androgens from other sources. That is when one must be looking for alternatives.The first thing should be trying to arrest the PSA down to remission levels. Dr. Myers uses a cocktail with leukine. You could do some researches on the second-line HT drugs used by famous oncologists. Ketoconazole or Zytiga with prednisone avoids the manufacturing of androgens at all levels in the body, including adrenal ones. The cancer itself for survival (Darwin natural selection principle) will produce and refine androgens at low levels but very potent (kind of DHT). Avodart and still better Xtandi work to avoid such refinement of androgens.
The multimodal principle is that cancer must be attacked from several fronts so that it has no chance to recuperate. In fact it goes against the sequentials used up to date in many oncology centres, the NCCN guidelines and the FDA. Cocktails seem to be the way for getting most out of a multimodal therapy in advanced difficult cases. These must be continuously supervised because of possible drugs interaction.
I know of a guy Gs9 that chose “the mother of all treatments”. He started with surgery plus chemo and continued with RT plus ADT, all in a series. He is doing OK with a PSA of less than 0.05. I think that you do not need the help of this “mother” but you should try getting the opinion of an oncologist of the grade of Scholz, Myers or Leibowitz. Your insurance may not cover the cost of the consultation; in any case you can follow the treatment at your local oncologist.
Prostate cancer cells may become more aggressive after been radiated. No one knows what will occur after RT because these affected cells maybe at the timing of mitosis or at the beginning of its life cycle. One may expect different occurrences depending on the timing when the DNA is damaged. The ones that cannot divide because of “bad copy” and die are the ones that may represent the success of the RT. The ones that “managed” to divide with its DNA intact may be the ones you name radio resistant. Chemo may work alike radiation destroying the DNA of cells causing the impossibility of dividing. The scale of a chemo therapy is worse because it affects the whole body (many side effects) while radiation is directional affecting the ones in its target.
I think of RT being instantaneous in its destruction (ionizing) of DNA. The results may take over one year to be seen. It all depends of the time cells take to duplicate in greater number with or without proper genetic materials, for one acertain conclusions.Looking into your latest PSA histology, I wonder if the result in January 0.34 is in fact the nadir in treatment terms. Your RT ended two month earlier in October, so that there was no down trend verified. The increase could be expected (as we discussed before) due to bounce. When in RT environment one should think that the ADT is not “acting” alone. To expect a lower PSA due to ADT administration is controversial. Inflammation commonly leads to erratic levels independently of the effects of the hormonal manipulations. I see your latest result of 6.43 meaningful in the overall analyses because the biopsy made your PSA going up even in the presence of the ADT effects.
Can you share the PSA and T levels before RT? I guess they were low too, due to ADT (mono therapy period).I know you are concerned with the increase and I am sorry if I cannot help you. All what I can give are lay opinions. I hope you find a decrease in PSA in three months time, after allowing the biopsy-inflammation to heal. I would suggest you to get by that time another image exam with C11-choline. This may rule out metastases in the lymph nodes (local) or at far places.
I also recommend you to get now a dexa scan and ecg, to monitor any trouble that ADT may cause in the future. Bisphosphonates are typically used in ADT protocols. Care for any deficiency in Vitamin D and be cautious for any anemia condition. These are common aspects in matters with cancer.
Losing of 40 Kg in 10 months is big. You need to care for diets recommended to PCa patients in treatment. Here is a link;
http://cancer.ucsf.edu/_docs/crc/nutrition_prostate.pdfBest wishes for improvements.
VGama
How about a trip to Portugal to enjoy the “real” Mediterranean diet and our wines. Let’s meet at the airport.
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PCa ChallengesMounty said:VG,
Thanks for your kind words and, as always, your valuable comments. A lot has happened during the 15 months since I last posted on the earlier thread. Because the recent post you're responding to was already quite long (and because I was worried some of the details might be unnecessarily worrisome for newly diagnosed Gleason 9 or 10 patients reading this post), I skipped over some of the details. Maybe this was a mistake - I'll try to summarize the additional data as succinctly as I can:
PSA reached a nadir of 0.34 ng/ml in January; it climbed back up to 0.55 in February, 1.09 in March, 2.01 in May and 2.59 in June, and last week's reading was 6.43, although this last reading is difficult to interpret for a few reasons, including the possibility it might have been influenced by the effects of a re-biopsy of the prostate on July 1 (more about this in a moment). We (the clinicians and I) thought this might be a bounce at first, but I don't think the steady climb in multiple readings over a period of 8 months is consistent with this possibility. I also should have told you that shortly after surgery at MSK last October to extract the tumor in my quadriceps, I was clobbered by acute, systemic pain in just about every skeletal joint in my body, most likely due to muscle wasting secondary to profound weight loss (I'm now more than 40 kilos lighter than I was 16 months ago), the inhibitory effects of ADT on muscle maintenance, and prolonged inactivity after the leg surgery. Part of the solution to this problem has been a steady diet of the potent prescription-only (at least in the States) NSAID Celebrex, 200 milligram capsules twice a day. I think you're correct that inflammation is one component of the problem, because immediately after I started taking Celebrex in March, the urinary symptoms improved, but only slightly. But Celebrex doesn't seem to have had a major impact on the PSA readings.
Perhaps the most important information I left out (and this was simply an oversight) is that 9 of 12 cores taken in the July 1 biopsy were positive for high-grade (Gleason 8 and 9) malignant disease. The meaning of this is complicated by the fact that biopsies performed such a short time after radiation treatment ends (10 months in my case) are likely detecting unresolved residual disease (radiation treatment can take up to a year or more to kill tumor cells) in addition to recurrent disease. Even so, the pathologists are apparently convinced that there is plenty of recurrent tumor, which is likely contributing to the rising PSA. Testosterone has been measured in parallel with every PSA measurement - it was down to 13 in January, and the latest reading is 3 (!) - and so the ADT drugs have been effectively doing their job of chemical castration. Combined with the evidence for castrate-resistant disease that was apparent at the start of this whole adventure, this is the basis for thinking that we're dealing with an extremely aggressive, castrate-resistant tumor. Whether it's also radiation-resistant (perhaps the more frequently employed term is radio-resistant but to me this is less descriptive) is less clear - this may simply reflect my occasional discouragement that after 16 months of very aggressive therapy (ADT + maximum radiation and I've also been on the anti-androgen Casodex since last October), not much seems to have been accomplished in the battle against this tumor.
The urinary problems that require continued catheterization are something of a mystery. Celebrex improved the situation, but not by much. A cystoscopy in February detected a radiation-induced stricture, which of course we assumed was responsible for the problem. Surgery (urethrotomy) a week later followed by repeated urethral dilations effectively eliminated this stricture, which was no longer detectable in a cystoscopy performed in June, and it modestly improved symptoms (increased urine flow), but not sufficient to stop catheterizing. This most recent cystoscopy also detected a kink in my urethra that the urologists think is caused by the tumor - so this suggests that the urethra is being occluded by pressure from the tumor. I'm not convinced, however, that (as you are suggesting), inflammation isn't also part of the problem, despite the Celebrex. But I'm also not sure how to address this possibility.
I have to tell you that maintaining a positive attitude about all this is easier in the absence of evidence for metastatic disease. The absence of metastatic disease in my case is quite extraordinary, and I suspect it has something to do with the fact that I'm extremely healthy in every other respect, perhaps because of an immune system that has always very effectively fought off infectious diseases. I also think that a sense of humor about all this stuff is important, although I'm having a little more difficulty maintaining one lately. Perhaps you and others who were posting on my earlier thread remember a fellow poster to this thread, Tp23, who has a very similar case. Tp23 and I (and our wives) have become close friends, and his wicked sense of humor (which was evident in the earlier thread) has helped both of us and our families to remain reasonably sane during the 16 months since we both learned we had been attacked by the bandit.
I would be grateful for any additional thoughts you might have now that you have a more complete understanding of the situation (hopefully). You are correct to note that both of us our amateurs in this business, which means that everyone reading our posts needs to evaluate the information content carefully. Even so, I believe that your posts have been equally as helpful as the advice of experts to many, many patients - certainly this is the case for me.
Bill
Hi Bill,Thx for your update. Sorry about the challenges you're facing as a G9 with a complex case. Your thoughtful articulate posts generate more questions than answers. The add'l info was helpful and may elicit better suggestions for follow-on salvage tx options.What were the results of your 3Tesla EMRI (Endorectal) last year? With PSA continuing to trend upwards now, wondering if the EMRI image study has been repeated in 2014 and compared to the 2013 MRI in terms of extent of ECE, i.e. local spread to SVs? To pelvic lymph nodes? Prostate size +/-? Hopefully the F-18 bone study you underwent was a F-18 Na (sodium) fused PET/CT (rather than another type of F-18 scan or Tech 99.Have you considered a consult with Dr Kwon at Mayo for the C-11 Choline imaging scan, as suggested in your first thread? With a rising PSA >2 after RT with adjuvant ADT & a rapid PSA doubling time, the C-11 Choline imaging study (although still considered experimental by some) may be an important test now in order to rule out mets in soft tissue as well as bone. Which ADT2 drug combination protocol are you currently taking and which ADT or other drugs, have you previously tried/failed?Thx for providing a more detailed PSA & T history. Was your DHT measured also? T converted to DHT via the adrenals and testes may be an even more potent fuel for PCa. That is why several of the top cutting edge PCa MOs Rx ADT3--the third component being a 5-ARI to address/inhibit DHT (dihydrotestosterone). Long term continuous use of ADT may raise the risk of metabolic syndrome and bone loss. Therefore, a baseline bone mineral density test with QCT and a full baseline cardio workup are recommended.What were the results of your 2nd opinion pathology on the initial 12 core biopsy sent to Epstein at JH for analysis? And also, on the re-biopsied cores sampled in July? Was Prostatic Small Cell Carcinoma (PSCC/neuroendocrine) and especially, ductal PCa ruled out by Epstein's PCa path lab at JH. Both variants are rare aggressive PCa's and, based on the info you've provided to date, those biopsy cores need to be carefully reevaluated by an expert 2nd opinion PCa path lab--Epstein. Were your two resected benign (?) tumors sent for a 2nd path opinion also, as they should be? Findings?You previously indicated you have 2 first degree family members with a dx of PCa. I wonder if you might share your father's and brother's PCa history & current status, i.e. age, treatments, remission, recurrence, salvage txs, HRPC, etc. This info may shed more light on your PCa gene pool.One doctor at your group conference commented about your case: "...given its early evolution to castrate-resistance and potential radiation-resistance, it's unlikely the tumor will respond very well to any new drugs we throw at it." At this early stage in your PCa tx journey, IMHO that is an unprofessional & irresponsible guesstimate at best (even if stated with good intention). Exactly which of the "any new drugs" is that 'doc' proposing be "thrown" at you!? When, if not now? And in what combination & sequential order?All things considered, it is imperative that your case be managed by a very, VERY (did I say 'very') knowledgeable, experienced, forward thinking & cutting edge PCa MO, such as Dr Myers (Virginia) and/or Dr Lam, Turner, or Scholz (SoCal). Google their names for info & websites. The SoCal Marina PCa grp does phone consults as well as in person appts.Depending on the outcome of C-11 imaging & add'l test results, etc., HDRBrachy (high dose rate brachytherapy) may be a viable salvage tx option vs salvage RP after failed primary RT. Along with newer second/third line drugs, including early adjuvant chemo intervention* (as you alluded to in your first thread re a clinical trial), multimodal salvage txs, spot RT for isolated mets, etc. may stall progression and hopefully manage chronic disease. See:That HW site link is another PCa social networking forum. It has lots of great PCa info, a very active & diverse contributing membership with excellent admin/mod oversight, and an efficient subject search feature:Short notice I know, but if possible...I highly recommend attending this years annual PCRI conference on PCa, Sept 5-7, at the Marriott near LAX in L.A., CA. Some of the internationally renown speakers/presenters at this years conf include Drs Kwon, Scholz, Moyad, Myers, Mulhall and others:I don't post on this site very much anymore. If you have questions, and I know you'll have lots of good ones, I urge you to make an appt ASAP with one of the top PCa MOs mentioned above to get those questions answered from a PCa medical expert, which I am not! This consult should include a thorough assessment of your case and a discussion re advanced drugs, imaging, salvage tx options, & clinical trials (PubMed).You seem to understand that your situation is complicated, but not hopeless. And the value of a sense of humor (laughter is the best medicine!) cannot be underestimated during tough stressful times. Good luck and best wishes as you go forward.M0 -
your comments and those by VGmrspjd said:PCa Challenges
Hi Bill,Thx for your update. Sorry about the challenges you're facing as a G9 with a complex case. Your thoughtful articulate posts generate more questions than answers. The add'l info was helpful and may elicit better suggestions for follow-on salvage tx options.What were the results of your 3Tesla EMRI (Endorectal) last year? With PSA continuing to trend upwards now, wondering if the EMRI image study has been repeated in 2014 and compared to the 2013 MRI in terms of extent of ECE, i.e. local spread to SVs? To pelvic lymph nodes? Prostate size +/-? Hopefully the F-18 bone study you underwent was a F-18 Na (sodium) fused PET/CT (rather than another type of F-18 scan or Tech 99.Have you considered a consult with Dr Kwon at Mayo for the C-11 Choline imaging scan, as suggested in your first thread? With a rising PSA >2 after RT with adjuvant ADT & a rapid PSA doubling time, the C-11 Choline imaging study (although still considered experimental by some) may be an important test now in order to rule out mets in soft tissue as well as bone. Which ADT2 drug combination protocol are you currently taking and which ADT or other drugs, have you previously tried/failed?Thx for providing a more detailed PSA & T history. Was your DHT measured also? T converted to DHT via the adrenals and testes may be an even more potent fuel for PCa. That is why several of the top cutting edge PCa MOs Rx ADT3--the third component being a 5-ARI to address/inhibit DHT (dihydrotestosterone). Long term continuous use of ADT may raise the risk of metabolic syndrome and bone loss. Therefore, a baseline bone mineral density test with QCT and a full baseline cardio workup are recommended.What were the results of your 2nd opinion pathology on the initial 12 core biopsy sent to Epstein at JH for analysis? And also, on the re-biopsied cores sampled in July? Was Prostatic Small Cell Carcinoma (PSCC/neuroendocrine) and especially, ductal PCa ruled out by Epstein's PCa path lab at JH. Both variants are rare aggressive PCa's and, based on the info you've provided to date, those biopsy cores need to be carefully reevaluated by an expert 2nd opinion PCa path lab--Epstein. Were your two resected benign (?) tumors sent for a 2nd path opinion also, as they should be? Findings?You previously indicated you have 2 first degree family members with a dx of PCa. I wonder if you might share your father's and brother's PCa history & current status, i.e. age, treatments, remission, recurrence, salvage txs, HRPC, etc. This info may shed more light on your PCa gene pool.One doctor at your group conference commented about your case: "...given its early evolution to castrate-resistance and potential radiation-resistance, it's unlikely the tumor will respond very well to any new drugs we throw at it." At this early stage in your PCa tx journey, IMHO that is an unprofessional & irresponsible guesstimate at best (even if stated with good intention). Exactly which of the "any new drugs" is that 'doc' proposing be "thrown" at you!? When, if not now? And in what combination & sequential order?All things considered, it is imperative that your case be managed by a very, VERY (did I say 'very') knowledgeable, experienced, forward thinking & cutting edge PCa MO, such as Dr Myers (Virginia) and/or Dr Lam, Turner, or Scholz (SoCal). Google their names for info & websites. The SoCal Marina PCa grp does phone consults as well as in person appts.Depending on the outcome of C-11 imaging & add'l test results, etc., HDRBrachy (high dose rate brachytherapy) may be a viable salvage tx option vs salvage RP after failed primary RT. Along with newer second/third line drugs, including early adjuvant chemo intervention* (as you alluded to in your first thread re a clinical trial), multimodal salvage txs, spot RT for isolated mets, etc. may stall progression and hopefully manage chronic disease. See:That HW site link is another PCa social networking forum. It has lots of great PCa info, a very active & diverse contributing membership with excellent admin/mod oversight, and an efficient subject search feature:Short notice I know, but if possible...I highly recommend attending this years annual PCRI conference on PCa, Sept 5-7, at the Marriott near LAX in L.A., CA. Some of the internationally renown speakers/presenters at this years conf include Drs Kwon, Scholz, Moyad, Myers, Mulhall and others:I don't post on this site very much anymore. If you have questions, and I know you'll have lots of good ones, I urge you to make an appt ASAP with one of the top PCa MOs mentioned above to get those questions answered from a PCa medical expert, which I am not! This consult should include a thorough assessment of your case and a discussion re advanced drugs, imaging, salvage tx options, & clinical trials (PubMed).You seem to understand that your situation is complicated, but not hopeless. And the value of a sense of humor (laughter is the best medicine!) cannot be underestimated during tough stressful times. Good luck and best wishes as you go forward.MVG and Mrs. PJD,
Thanks very much again for your comments and insightful questions – I’m happy to hear from both of you again. Twice in the last day I’ve worked for an hour or so on a response that addresses your questions and comments in detail and then saw my text disappear with an errant mouse click. I’m going to try again (with wordprocessing software this time). I apologize for the length.
A month after the onset of ADT, PSA had declined to 26 (from 34) and a month later (at the onset of RT), it was 13. Usually PSA declines by 80% or more within the first 30 days after ADT commences. After RT PSA went from 6 to 1 in three sequential readings in October, November and December before it finally bottomed out at 0.34 in January. (VG, radiation treatment ended in August rather than October, so the interval to nadir was four months, not two.) Combined with the steady increase since then and the absence of erratic fluctuations at any point, I think this means the 0.34 reading in January really was a post radiation nadir. I'm guessing that the absence of erratic fluctuations in PSA as it steadily decreased and then increased again over a period of months argues against post-radiation bounce or some other sporadic factor, like inflammation (although I agree with you VG that inflammation may be contributing).
With regard to questions about a genetic component to the disease, a month ago my wife and I met with a genetics counselor to discuss my extensive family cancer history (early onset Pca diagnosis (Gleason 6, age 41) for a younger brother (a radical RP 11 years ago solved his problem), Pca diagnosis at age 70 in our Dad, who may have had an aggressive tumor but died six years later of other problems; early onset uterine cancer diagnosis in a younger sister (sometime in her 30s; she’s now in her early fifties and is healthy), early onset breast cancer diagnosis in our Mom, who died of breast cancer; and numerous cases of early onset disease in siblings of my parents (all five of my mother’s siblings died of cancer). This history certainly points to a heritable genetic component. A screen ordered by the genetics counselor of my DNA for germline mutations in 30 genes that predispose to cancer is underway. It’s possible this screen may identify a common denominator between the prostate tumor and the two benign tumors.
VG – note that Casodex was withdrawn about a month ago – we expect (or hope anyway) to see a decline in PSA and slower progression via the mechanism you describe, but won’t know for several weeks until the effects of the recent biopsy and a recent UTI are resolved. Mrs. PJD – regarding your question about second opinions on the pathology of the primary and imaging studies – I think with this question you’re confusing me with someone else who obtained a second opinion from Epstein at JH regarding their primary. The cores harvested from my prostate last year were read by three sets of pathologists, including those at my institution and pathologists at MSKCC, but not Johns Hopkins. All concurred on the diagnosis of prostatic adenocarcinoma. The biopsy of the leg tumor was not definitive, but pathology of the tumor after it was resected by surgeons at MSK clearly indicated a benign tumor, which is consistent with the earlier diagnosis based on imaging studies by sarcoma doctors where I work. The cores from the re-biopsy of the prostate in July or of the rib tumor have not been read by a second set of pathologists. Last year’s MRI of the pelvic region indicated SV involvement, but not lymph nodes. This year’s MRI shortly before the re-biopsy failed to detect lymph node involvement this year as well.
Recent discussions with clinicians of treatment possibilities going forward (in addition to Casodex withdrawal) have focused on four options: 1. salvage radical prostatectomy; 2. debulking surgery; 3. second-line ADT, including abiraterone and/or enzalutamide, and 4. immunotherapy (Provenge). Both the latter two options would be good ones except that they’re not approved for nonmetastatic disease, and I’m not yet metastatic (thank God! – but it’s ironic that if I had not had the rib yanked out and biopsied, the positive bone scans that detected the rib lesion probably would have been sufficient to convince my insurance company that I was metastatic, and therefore eligible for any of these expensive options. (Most of the clinicians assumed the lesion was metastatic and one even argued I should not bother to have the rib resected because he was certain this was the case – I don’t think anyone was seriously considering the possibility of a third unrelated tumor). Although I’m extremely happy to be nonmetastatic, this puts us in kind of a tough spot – unlike many other patients who are castrate-resistant, but not metastatic, I’m dealing with an extremely aggressive tumor that’s throwing out PSA at a rapid rate usually seen only in aggressive systemic disease, and more often in much older men. This is creating a sense of urgency about the situation, which I think is what’s driving the argument for many of the clinicians for the surgery options, despite the risks (the vote at the conference was 9 for surgery and 3 against, not the 6 vs. 3 I indicated to VG earlier).
At the moment I’m disinclined to go with either of the surgery options that have been proposed (salvage RP or debulking), but I haven’t ruled them out – although I’ve also told our friend Tp23 (from last year’s thread) that if I eventually choose surgery, he should whack me on the head with a 2 X 4 until I come to my senses. I’m willing to risk the permanent complications that would likely result if I thought the chance I would be rid of disease was reasonably high, but it’s not. The worst outcome would be permanent bowel and urinary incontinence due to the surgery followed by the onset of aggressive metastatic disease six months later.
To be honest, I posted to this forum again partly because I’m suffering from fatigue associated with the seemingly endless process of looking for answers to tough questions (Mrs. PJD, you may recall that you lectured me on this topic last year, and it was a very valuable lesson). I was hoping that someone reading my posts would come to the rescue and tell me, “OK, this is what you need to do” and why and then I can just do it, no more questions asked. This is not the way this stuff sometimes works, of course, especially not with complicated cases like mine. I did, however, momentarily lose sight of the appropriate questions, and this is where both of you have been enormously helpful once again with your recent posts. It did not occur to me, for example, that the prostate tumor could be evolving into something more aggressive than an adenocarcinoma, or that the read on the rib biopsy might be wrong - and so a second opinion on the re-biopsy cores and the rib slides is warranted. This is a key point, and I’m making arrangements for additional independent reads. It also didn’t occur to me (and I don’t know why other than fatigue!) that if we’re dealing with a prostate tumor that’s evolved into something other than an adenocarcinoma, the source of the rapidly rising PSA could be soft tissue mets, which we haven’t looked for. I was thinking that the F-18 (NaCl) bone scan (which was in fact a PET/CT scan) was sufficient. Both of you suggested a C-11 scan, which I had been dismissing as unnecessary but now I realize this was a mistake. It also did not occur to me that measuring DHT might be informative – I’ll bring this up with the clinicians. I know very little about HDR Brachytherapy, which has not been discussed (or ruled out) by the clinicians – I’m now looking into it.
VG – you are absolutely correct that it was a mistake to hold back in my previous post on details of my case for the reason I stated. I agree that this forum works so well because of the free exchange of information. In fact, I’m hoping that this thread will be helpful to others with advanced cases like mine – as we discussed last year, VG, too often those with advanced cases at diagnosis don’t post to this forum, and I feel badly that I stopped posting for more than a year. For others in the same boat but are more recently diagnosed, some of the terminology VG and Mrs. PJD and I are using may not yet be familiar to you. I’m happy to answer any questions you might have.
Thanks again VG and Mrs. PJD – this has been a big help. Let me know if you have any additional suggestions or questions. I’ll post on progress in the future.
P.S. I think you are correct, Mrs. PJD, that the clinician’s comment that “throwing new drugs” at the problem would not have much of an effect would be unprofessional, but only in other contexts (an office visit between patient and clinician, for example). But in this case, I think it was OK. It was made at a clinical conference that involved a spirited debate about my case that reflected the clinicians’ frustrations as well as mine. It was directed at other clinicians more than it was at me. VG, the best medicine might be a trip to Portugal, which I’m planning to make when I can. I will keep you posted on this as well!
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I am happy to see that UCSFVascodaGama said:Multimodal approach
Bill
I am sorry for the comments on your status. I did not know the details and just wanted to pass you some hits that could be of help in your decisions. You are consulting a good team of physicians and they know well what the best is for you. Dr. Susan Slovin, a medical oncologist and researcher at the MSKCC, gave me precious suggestions when I recurred after surgery (2001) during a nasty “foggy” period of my journey.
I disagree with your concern for posting all the information regarding your case. The worse for cancer patients is not knowing about real facts. I correspond to other PCa forums too, but I like the CSN because it is free of “restrictions”. We can share more openly the details and aspects evolving our problem. It is good to read plain stories of the many survivors, even the nasty ones. It makes us to be more respectful to one another and become closer in the common matter.
Many of you, physicians, for whatever reason it may be, think that we patients are better if kept in the “dark”, so you tend not to be so descriptive or disclose the “baddy” of the story. However, in this forum we go against that principle and discuss openly the feelings even when complaining about our doctor’s appointments and views. Surely you are welcome with or without the concerns.You got a very difficult cancer to treat. The initial diagnosis with Gleason 9 and voluminous tumour (14 positive cores) plus positive DRE (suggesting extraprostatic invasion) made you to choose RT+ADT. I think you did well. Your fight is still going on and you need to get to a decision with the intent in holding any progression.
Your exchanged posts with Casey (http://csn.cancer.org/node/258414#comment-1368807) on the multimodal therapy approach are a good start to look at for your continuing treatment. I do not suggest surgery yet because of the loss in quality of life and because of the timing so close to RT (8 months). You can do it at a later date as the action would be debulking the gland, which in the presence of ECE does not assure complete cure but longer survival. With that in view, surgery can be done any time, though, keeping in mind that in a later date would allow the cancer to spread further (if nothing is done in-between). The recent negative image exams may consider your case localized yet.When a case becomes hormone refractory while a guy is having a traditional ADT protocol, it is so considered because the cancer starts using drugs like Casodex (antiandrogens) to satisfy its own food demand. These drugs got similar bio structures as the real stuff and they are available plenty (one is taking it) to feed on. Stopping Casodex one may experience the so called AAWR (withdrawing response). Hormone refractory in such a case should be termed antiandrogen refractory not ADA refractory.
Continuing with a LHRH agonist seems proper because it avoids the circulating testosterone. But it does not stop the cancer from availing androgens from other sources. That is when one must be looking for alternatives.The first thing should be trying to arrest the PSA down to remission levels. Dr. Myers uses a cocktail with leukine. You could do some researches on the second-line HT drugs used by famous oncologists. Ketoconazole or Zytiga with prednisone avoids the manufacturing of androgens at all levels in the body, including adrenal ones. The cancer itself for survival (Darwin natural selection principle) will produce and refine androgens at low levels but very potent (kind of DHT). Avodart and still better Xtandi work to avoid such refinement of androgens.
The multimodal principle is that cancer must be attacked from several fronts so that it has no chance to recuperate. In fact it goes against the sequentials used up to date in many oncology centres, the NCCN guidelines and the FDA. Cocktails seem to be the way for getting most out of a multimodal therapy in advanced difficult cases. These must be continuously supervised because of possible drugs interaction.
I know of a guy Gs9 that chose “the mother of all treatments”. He started with surgery plus chemo and continued with RT plus ADT, all in a series. He is doing OK with a PSA of less than 0.05. I think that you do not need the help of this “mother” but you should try getting the opinion of an oncologist of the grade of Scholz, Myers or Leibowitz. Your insurance may not cover the cost of the consultation; in any case you can follow the treatment at your local oncologist.
Prostate cancer cells may become more aggressive after been radiated. No one knows what will occur after RT because these affected cells maybe at the timing of mitosis or at the beginning of its life cycle. One may expect different occurrences depending on the timing when the DNA is damaged. The ones that cannot divide because of “bad copy” and die are the ones that may represent the success of the RT. The ones that “managed” to divide with its DNA intact may be the ones you name radio resistant. Chemo may work alike radiation destroying the DNA of cells causing the impossibility of dividing. The scale of a chemo therapy is worse because it affects the whole body (many side effects) while radiation is directional affecting the ones in its target.
I think of RT being instantaneous in its destruction (ionizing) of DNA. The results may take over one year to be seen. It all depends of the time cells take to duplicate in greater number with or without proper genetic materials, for one acertain conclusions.Looking into your latest PSA histology, I wonder if the result in January 0.34 is in fact the nadir in treatment terms. Your RT ended two month earlier in October, so that there was no down trend verified. The increase could be expected (as we discussed before) due to bounce. When in RT environment one should think that the ADT is not “acting” alone. To expect a lower PSA due to ADT administration is controversial. Inflammation commonly leads to erratic levels independently of the effects of the hormonal manipulations. I see your latest result of 6.43 meaningful in the overall analyses because the biopsy made your PSA going up even in the presence of the ADT effects.
Can you share the PSA and T levels before RT? I guess they were low too, due to ADT (mono therapy period).I know you are concerned with the increase and I am sorry if I cannot help you. All what I can give are lay opinions. I hope you find a decrease in PSA in three months time, after allowing the biopsy-inflammation to heal. I would suggest you to get by that time another image exam with C11-choline. This may rule out metastases in the lymph nodes (local) or at far places.
I also recommend you to get now a dexa scan and ecg, to monitor any trouble that ADT may cause in the future. Bisphosphonates are typically used in ADT protocols. Care for any deficiency in Vitamin D and be cautious for any anemia condition. These are common aspects in matters with cancer.
Losing of 40 Kg in 10 months is big. You need to care for diets recommended to PCa patients in treatment. Here is a link;
http://cancer.ucsf.edu/_docs/crc/nutrition_prostate.pdfBest wishes for improvements.
VGama
How about a trip to Portugal to enjoy the “real” Mediterranean diet and our wines. Let’s meet at the airport.
I am happy to see that UCSF (one of the leaders in diet) are now supporting more of a plant base diet that I incorporated 5 years ago in my fight against this beast...I only disagree with their statements/studies on the the use of soy products (I never eat soy unless it is fermented-if interested follow Dr Mercola diet tips)....
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High Risk PCaMounty said:your comments and those by VG
VG and Mrs. PJD,
Thanks very much again for your comments and insightful questions – I’m happy to hear from both of you again. Twice in the last day I’ve worked for an hour or so on a response that addresses your questions and comments in detail and then saw my text disappear with an errant mouse click. I’m going to try again (with wordprocessing software this time). I apologize for the length.
A month after the onset of ADT, PSA had declined to 26 (from 34) and a month later (at the onset of RT), it was 13. Usually PSA declines by 80% or more within the first 30 days after ADT commences. After RT PSA went from 6 to 1 in three sequential readings in October, November and December before it finally bottomed out at 0.34 in January. (VG, radiation treatment ended in August rather than October, so the interval to nadir was four months, not two.) Combined with the steady increase since then and the absence of erratic fluctuations at any point, I think this means the 0.34 reading in January really was a post radiation nadir. I'm guessing that the absence of erratic fluctuations in PSA as it steadily decreased and then increased again over a period of months argues against post-radiation bounce or some other sporadic factor, like inflammation (although I agree with you VG that inflammation may be contributing).
With regard to questions about a genetic component to the disease, a month ago my wife and I met with a genetics counselor to discuss my extensive family cancer history (early onset Pca diagnosis (Gleason 6, age 41) for a younger brother (a radical RP 11 years ago solved his problem), Pca diagnosis at age 70 in our Dad, who may have had an aggressive tumor but died six years later of other problems; early onset uterine cancer diagnosis in a younger sister (sometime in her 30s; she’s now in her early fifties and is healthy), early onset breast cancer diagnosis in our Mom, who died of breast cancer; and numerous cases of early onset disease in siblings of my parents (all five of my mother’s siblings died of cancer). This history certainly points to a heritable genetic component. A screen ordered by the genetics counselor of my DNA for germline mutations in 30 genes that predispose to cancer is underway. It’s possible this screen may identify a common denominator between the prostate tumor and the two benign tumors.
VG – note that Casodex was withdrawn about a month ago – we expect (or hope anyway) to see a decline in PSA and slower progression via the mechanism you describe, but won’t know for several weeks until the effects of the recent biopsy and a recent UTI are resolved. Mrs. PJD – regarding your question about second opinions on the pathology of the primary and imaging studies – I think with this question you’re confusing me with someone else who obtained a second opinion from Epstein at JH regarding their primary. The cores harvested from my prostate last year were read by three sets of pathologists, including those at my institution and pathologists at MSKCC, but not Johns Hopkins. All concurred on the diagnosis of prostatic adenocarcinoma. The biopsy of the leg tumor was not definitive, but pathology of the tumor after it was resected by surgeons at MSK clearly indicated a benign tumor, which is consistent with the earlier diagnosis based on imaging studies by sarcoma doctors where I work. The cores from the re-biopsy of the prostate in July or of the rib tumor have not been read by a second set of pathologists. Last year’s MRI of the pelvic region indicated SV involvement, but not lymph nodes. This year’s MRI shortly before the re-biopsy failed to detect lymph node involvement this year as well.
Recent discussions with clinicians of treatment possibilities going forward (in addition to Casodex withdrawal) have focused on four options: 1. salvage radical prostatectomy; 2. debulking surgery; 3. second-line ADT, including abiraterone and/or enzalutamide, and 4. immunotherapy (Provenge). Both the latter two options would be good ones except that they’re not approved for nonmetastatic disease, and I’m not yet metastatic (thank God! – but it’s ironic that if I had not had the rib yanked out and biopsied, the positive bone scans that detected the rib lesion probably would have been sufficient to convince my insurance company that I was metastatic, and therefore eligible for any of these expensive options. (Most of the clinicians assumed the lesion was metastatic and one even argued I should not bother to have the rib resected because he was certain this was the case – I don’t think anyone was seriously considering the possibility of a third unrelated tumor). Although I’m extremely happy to be nonmetastatic, this puts us in kind of a tough spot – unlike many other patients who are castrate-resistant, but not metastatic, I’m dealing with an extremely aggressive tumor that’s throwing out PSA at a rapid rate usually seen only in aggressive systemic disease, and more often in much older men. This is creating a sense of urgency about the situation, which I think is what’s driving the argument for many of the clinicians for the surgery options, despite the risks (the vote at the conference was 9 for surgery and 3 against, not the 6 vs. 3 I indicated to VG earlier).
At the moment I’m disinclined to go with either of the surgery options that have been proposed (salvage RP or debulking), but I haven’t ruled them out – although I’ve also told our friend Tp23 (from last year’s thread) that if I eventually choose surgery, he should whack me on the head with a 2 X 4 until I come to my senses. I’m willing to risk the permanent complications that would likely result if I thought the chance I would be rid of disease was reasonably high, but it’s not. The worst outcome would be permanent bowel and urinary incontinence due to the surgery followed by the onset of aggressive metastatic disease six months later.
To be honest, I posted to this forum again partly because I’m suffering from fatigue associated with the seemingly endless process of looking for answers to tough questions (Mrs. PJD, you may recall that you lectured me on this topic last year, and it was a very valuable lesson). I was hoping that someone reading my posts would come to the rescue and tell me, “OK, this is what you need to do” and why and then I can just do it, no more questions asked. This is not the way this stuff sometimes works, of course, especially not with complicated cases like mine. I did, however, momentarily lose sight of the appropriate questions, and this is where both of you have been enormously helpful once again with your recent posts. It did not occur to me, for example, that the prostate tumor could be evolving into something more aggressive than an adenocarcinoma, or that the read on the rib biopsy might be wrong - and so a second opinion on the re-biopsy cores and the rib slides is warranted. This is a key point, and I’m making arrangements for additional independent reads. It also didn’t occur to me (and I don’t know why other than fatigue!) that if we’re dealing with a prostate tumor that’s evolved into something other than an adenocarcinoma, the source of the rapidly rising PSA could be soft tissue mets, which we haven’t looked for. I was thinking that the F-18 (NaCl) bone scan (which was in fact a PET/CT scan) was sufficient. Both of you suggested a C-11 scan, which I had been dismissing as unnecessary but now I realize this was a mistake. It also did not occur to me that measuring DHT might be informative – I’ll bring this up with the clinicians. I know very little about HDR Brachytherapy, which has not been discussed (or ruled out) by the clinicians – I’m now looking into it.
VG – you are absolutely correct that it was a mistake to hold back in my previous post on details of my case for the reason I stated. I agree that this forum works so well because of the free exchange of information. In fact, I’m hoping that this thread will be helpful to others with advanced cases like mine – as we discussed last year, VG, too often those with advanced cases at diagnosis don’t post to this forum, and I feel badly that I stopped posting for more than a year. For others in the same boat but are more recently diagnosed, some of the terminology VG and Mrs. PJD and I are using may not yet be familiar to you. I’m happy to answer any questions you might have.
Thanks again VG and Mrs. PJD – this has been a big help. Let me know if you have any additional suggestions or questions. I’ll post on progress in the future.
P.S. I think you are correct, Mrs. PJD, that the clinician’s comment that “throwing new drugs” at the problem would not have much of an effect would be unprofessional, but only in other contexts (an office visit between patient and clinician, for example). But in this case, I think it was OK. It was made at a clinical conference that involved a spirited debate about my case that reflected the clinicians’ frustrations as well as mine. It was directed at other clinicians more than it was at me. VG, the best medicine might be a trip to Portugal, which I’m planning to make when I can. I will keep you posted on this as well!
Dr Jon Epstein at JH is one of the best expert pathologists (if not The best IMHO) specializing in biopsied PCa tumor/tissue analysis.Perhaps you misunderstood as I wasn't confusing you with another patient--I was subtly suggesting that due to your complex case your prostate biopsy cores (from 2013 & 2014) & the recently resected tumors all be reevaluated (to rule out rare aggressive PCa variants) by a highly respected, published pathologist who specializes in PCa pathology--that being Dr Epstein.I can appreciate your view of that one Dr in your group conference. Still, the comment is unprofessional & a guesstimate, no matter who it was directed at. The important questions left unanswered are valid & need answers from that doc and your conference team prior to a recommendation vote for salvage debulking RP--Exactly which of the "any new drugs" are they proposing be "thrown" at you!? When, if not now? And in what combination & sequential order? If they can't or won't provide those answers, it's time to go elsewhere, even if you have to sacrifice the convenience of walking down the hall for a medical appt. Who ever said that PCa would be convenient?Earlier rather than late chemo intervention is a more recent multimodal tx protocol in high risk cases such as G9's, including those who show no met findings on imaging (or advanced imaging such as C-11 and F-18 PET/CT). In 2010 a good friend of ours was dx'd as G9 with high risk features and NO mets. His multimodal txs were managed by a well known MO (medical oncologist) specializing in PCa who added an unconventional (at that time) adjuvant chemo protocol early on with his other txs. His case was complex and did not include primary RP or salvage RP for debulking. Today, 4 years out from dx/txs (diagnosis/treatments), he is doing well, with his chronic disease closely supervised & managed by independent PCa MOs, even though txs were taken at a large teaching hospital/center of excellence. Certainly this is only one anecdotal case, but gotta say for him, so far so good!Of course, every case is unique and you are your own best medical advocate. If you seriously would like add'l perspectives/thoughts from others, including from actual G9's with complex cases, check HW. There are several active members posting there who have experience with early chemo tx protocol, some in clinical trial. Couldn't hurt and could provide add'l info about your case that you're seeking from others, including from those who have been where you are now.Of course, as a scientist you know that info on social networking cancer sites like these can be interesting and sometimes useful but, it should never be a substitution for your own independent research from reputable PCa medical websites/resources. A few research sites we used:Hope this is helpful to others dx'd with high risk PCa.MWife of a PCa Survivor, T3 stage, locally advanced, high risk. Approaching 5 years in remission.0 -
High Risk PCamrspjd said:High Risk PCa
Dr Jon Epstein at JH is one of the best expert pathologists (if not The best IMHO) specializing in biopsied PCa tumor/tissue analysis.Perhaps you misunderstood as I wasn't confusing you with another patient--I was subtly suggesting that due to your complex case your prostate biopsy cores (from 2013 & 2014) & the recently resected tumors all be reevaluated (to rule out rare aggressive PCa variants) by a highly respected, published pathologist who specializes in PCa pathology--that being Dr Epstein.I can appreciate your view of that one Dr in your group conference. Still, the comment is unprofessional & a guesstimate, no matter who it was directed at. The important questions left unanswered are valid & need answers from that doc and your conference team prior to a recommendation vote for salvage debulking RP--Exactly which of the "any new drugs" are they proposing be "thrown" at you!? When, if not now? And in what combination & sequential order? If they can't or won't provide those answers, it's time to go elsewhere, even if you have to sacrifice the convenience of walking down the hall for a medical appt. Who ever said that PCa would be convenient?Earlier rather than late chemo intervention is a more recent multimodal tx protocol in high risk cases such as G9's, including those who show no met findings on imaging (or advanced imaging such as C-11 and F-18 PET/CT). In 2010 a good friend of ours was dx'd as G9 with high risk features and NO mets. His multimodal txs were managed by a well known MO (medical oncologist) specializing in PCa who added an unconventional (at that time) adjuvant chemo protocol early on with his other txs. His case was complex and did not include primary RP or salvage RP for debulking. Today, 4 years out from dx/txs (diagnosis/treatments), he is doing well, with his chronic disease closely supervised & managed by independent PCa MOs, even though txs were taken at a large teaching hospital/center of excellence. Certainly this is only one anecdotal case, but gotta say for him, so far so good!Of course, every case is unique and you are your own best medical advocate. If you seriously would like add'l perspectives/thoughts from others, including from actual G9's with complex cases, check HW. There are several active members posting there who have experience with early chemo tx protocol, some in clinical trial. Couldn't hurt and could provide add'l info about your case that you're seeking from others, including from those who have been where you are now.Of course, as a scientist you know that info on social networking cancer sites like these can be interesting and sometimes useful but, it should never be a substitution for your own independent research from reputable PCa medical websites/resources. A few research sites we used:Hope this is helpful to others dx'd with high risk PCa.MWife of a PCa Survivor, T3 stage, locally advanced, high risk. Approaching 5 years in remission.In fact I did not understand the subtlety of your earlier question of what Dr. Jon Epstein’s at Johns Hopkins take was on the earlier prostate tumor biopsy, which as I indicated earlier, was analyzed by three sets of pathologists, including those at my institution and at MSKCC, but not pathologists at JH. It’s difficult to parse the information content of subtle comments like yours made in a forum that I expect to involve straightforward information. Perhaps Dr. Epstein is “the best”, as you suggest, but I rely on far more information than the suggestions of anonymous contributors to forums like this one when making decisions about which experts are best to assess the clinical data relevant to my case, and I think this process should be respected. Social networking cancer forums like this one are, in fact, useful, but in my case they certainly haven’t been a substitute for medical websites and other resources that contain more rigorously evaluated information, which is especially easy for me to access as a scientist. One reason I haven’t posted at this forum for more than a year is because of the amount of time I’ve spent tracking down information elsewhere. In any case, your earlier posts identified some useful approaches that I had not considered – this one, not so much. I’m not sure exactly what I said that deserved this response.
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High Risk Aggressive PCaMounty said:High Risk PCa
In fact I did not understand the subtlety of your earlier question of what Dr. Jon Epstein’s at Johns Hopkins take was on the earlier prostate tumor biopsy, which as I indicated earlier, was analyzed by three sets of pathologists, including those at my institution and at MSKCC, but not pathologists at JH. It’s difficult to parse the information content of subtle comments like yours made in a forum that I expect to involve straightforward information. Perhaps Dr. Epstein is “the best”, as you suggest, but I rely on far more information than the suggestions of anonymous contributors to forums like this one when making decisions about which experts are best to assess the clinical data relevant to my case, and I think this process should be respected. Social networking cancer forums like this one are, in fact, useful, but in my case they certainly haven’t been a substitute for medical websites and other resources that contain more rigorously evaluated information, which is especially easy for me to access as a scientist. One reason I haven’t posted at this forum for more than a year is because of the amount of time I’ve spent tracking down information elsewhere. In any case, your earlier posts identified some useful approaches that I had not considered – this one, not so much. I’m not sure exactly what I said that deserved this response.
Not sure what upset you as nothing I wrote was meant to do so. Sorry you took it that way and out of context. I could say the same thing--that I’m not sure exactly what I said that deserved your unkind response, subtle or not.
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High Risk PCamrspjd said:High Risk Aggressive PCa
Not sure what upset you as nothing I wrote was meant to do so. Sorry you took it that way and out of context. I could say the same thing--that I’m not sure exactly what I said that deserved your unkind response, subtle or not.
Mrs. PJD - I really didn't understand your post but it also was a difficult day and I should have waited for the smoke to clear before I posted. I'm sorry. Your help is much appreciated. Bill
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Your real status
Bill
You are in the good track. You got the puzzle pieces and now you need to set them into the right places.
I read above in one of your posts that you will make a decision, starting with an investigation on your present “real” status. What kind of cancer cells do I have and to which extent is the cancer localized. This is important to know before you continue with any aggressive radical treatment, with intent at cure.
With your latest information regarding the time of HT and RT and tests, I would think that you have an earlier recurrence, but ………… ???????????? …………………… there could be some doubts in the judgement of the biochemical failure. There are no statistics for levels of PSA in combo treatments (RT+HT) but a much lower level and faster should be expected to occur after neoadjuvant HT plus RT. If RT has been alone in the setting, the “fast drop” of PSA after RT would be related to RT failure (decreases less than 12 months are linked with earlier recurrences). This could be judged that the cancer is not just localized. How to find its hidden place should take prime attention.
Interestingly, if the cancer is found at fewer places (your above comment) you still got a good weapon to kill the bandit. Spot RT is possible at some places as far as its newer location does not fall within the field of previous isodose planning. At the same area, RT is not recommended for a period of 5 years (norms of tissue radiation absorption limits). The danger would be fistulas. Another salvage treatment to consider after radiation treatments is cryotherapy to freeze the prostate gland to kill any remaining cancer cells. Salvage surgery is always controversial. A renowned professor and expert in medical oncology and urologic cance says this;
Some highly skilled surgeons can perform a salvage prostatectomy, but the larger consideration is whether it is worth doing at all. One could make a strong argument that in most cases, rising PSA after radiation therapy indicates systemic disease, and any type of local therapy — even salvage prostatectomy — is not going to solve the larger problem of cancer cells that have metastasized elsewhere. For those cells, you need hormone therapy
In any case, if the continuing therapy is that for the destruction of the DNA (your family cancer genetics), chemo may be useful at this stage. I would suggest you to do some researches (common to you as a scientist, right?) into the matter while waiting for the above discussed tests and exams. Look for the latest chemo compounds (eg; Jevtana, etc), and find out about the useful typical additions to HT protocols such as; leukine for reinforcement of the immune, revlimid, emcyt, thalidomide and angiostatin for avoiding formation of new blood vessels, samarium, and strontium to reinforce bone avoiding those cysts that can turn PCa, etc.
Drugs that complement CAD protocols could include; Proscar (5-ARI), Celebrex (anti-inflammatory), Calcitriol (vit D). You may also add Climera patches to counter the side effects from hypogonadism.Another though is the use of estrogens in your case with female related cancer family. DES is something in use around the world but not so frenzy in the USA. You could use patches on/off periods and control the period with levels of PSA.
Independently of what you are going to take, I would suggest you to add more tests to your periodical PSA+T, for means of monitoring and control. These biomarkers are secreted by cancers similar to your conditions. These are; PAP (prostatic acid phosphatase), CEA (carcinoembryonic antigen), NSE (neuron specific enolase) and CGA (chromogranin A).
I am giving you a good set of home work. This is easy for you to solve because of your close medical “family”. I am sorry if some members of this forum are straight forward with opinions that may hurt the feelings. We all want just to help. You are passing a bad chapter in your life, but it will improve. I would recommend you to continue this thread posting at the end not in between to get a better narration and understanding of our discussions.
Best wishes and luck in the decisions ahead.
VGama
Come on. The Autumn may be the best timing for visiting Tras-os-Montes e Alto Douro and enjoy the local produces. Regain of Peace of Mind is assured.
0 -
Your real statusVascodaGama said:Your real status
Bill
You are in the good track. You got the puzzle pieces and now you need to set them into the right places.
I read above in one of your posts that you will make a decision, starting with an investigation on your present “real” status. What kind of cancer cells do I have and to which extent is the cancer localized. This is important to know before you continue with any aggressive radical treatment, with intent at cure.
With your latest information regarding the time of HT and RT and tests, I would think that you have an earlier recurrence, but ………… ???????????? …………………… there could be some doubts in the judgement of the biochemical failure. There are no statistics for levels of PSA in combo treatments (RT+HT) but a much lower level and faster should be expected to occur after neoadjuvant HT plus RT. If RT has been alone in the setting, the “fast drop” of PSA after RT would be related to RT failure (decreases less than 12 months are linked with earlier recurrences). This could be judged that the cancer is not just localized. How to find its hidden place should take prime attention.
Interestingly, if the cancer is found at fewer places (your above comment) you still got a good weapon to kill the bandit. Spot RT is possible at some places as far as its newer location does not fall within the field of previous isodose planning. At the same area, RT is not recommended for a period of 5 years (norms of tissue radiation absorption limits). The danger would be fistulas. Another salvage treatment to consider after radiation treatments is cryotherapy to freeze the prostate gland to kill any remaining cancer cells. Salvage surgery is always controversial. A renowned professor and expert in medical oncology and urologic cance says this;
Some highly skilled surgeons can perform a salvage prostatectomy, but the larger consideration is whether it is worth doing at all. One could make a strong argument that in most cases, rising PSA after radiation therapy indicates systemic disease, and any type of local therapy — even salvage prostatectomy — is not going to solve the larger problem of cancer cells that have metastasized elsewhere. For those cells, you need hormone therapy
In any case, if the continuing therapy is that for the destruction of the DNA (your family cancer genetics), chemo may be useful at this stage. I would suggest you to do some researches (common to you as a scientist, right?) into the matter while waiting for the above discussed tests and exams. Look for the latest chemo compounds (eg; Jevtana, etc), and find out about the useful typical additions to HT protocols such as; leukine for reinforcement of the immune, revlimid, emcyt, thalidomide and angiostatin for avoiding formation of new blood vessels, samarium, and strontium to reinforce bone avoiding those cysts that can turn PCa, etc.
Drugs that complement CAD protocols could include; Proscar (5-ARI), Celebrex (anti-inflammatory), Calcitriol (vit D). You may also add Climera patches to counter the side effects from hypogonadism.Another though is the use of estrogens in your case with female related cancer family. DES is something in use around the world but not so frenzy in the USA. You could use patches on/off periods and control the period with levels of PSA.
Independently of what you are going to take, I would suggest you to add more tests to your periodical PSA+T, for means of monitoring and control. These biomarkers are secreted by cancers similar to your conditions. These are; PAP (prostatic acid phosphatase), CEA (carcinoembryonic antigen), NSE (neuron specific enolase) and CGA (chromogranin A).
I am giving you a good set of home work. This is easy for you to solve because of your close medical “family”. I am sorry if some members of this forum are straight forward with opinions that may hurt the feelings. We all want just to help. You are passing a bad chapter in your life, but it will improve. I would recommend you to continue this thread posting at the end not in between to get a better narration and understanding of our discussions.
Best wishes and luck in the decisions ahead.
VGama
Come on. The Autumn may be the best timing for visiting Tras-os-Montes e Alto Douro and enjoy the local produces. Regain of Peace of Mind is assured.
VG, I've been struggling to find the time to respond but rest assured, I'm doing my homework! My wife and I are flying to New York tomorrow for a meeting on Monday with a medical oncologist at MSKCC. Going into this meeting I have a much better understanding of the questions to ask thanks to you and Mrs. PJD.
Best wishes,
Bill
0
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